Accès gratuit
Numéro
Med Sci (Paris)
Volume 28, Numéro 3, Mars 2012
Page(s) 288 - 296
Section Vieillissement
DOI https://doi.org/10.1051/medsci/2012283017
Publié en ligne 6 avril 2012
  1. Hayflick L. The limited in vitro lifetime of human diploid cell strains. Exp Cell Res 1965 ; 37 : 614–636. [CrossRef] [PubMed] [Google Scholar]
  2. Gire V. La sénescence : une barrière télomérique à l’immortalité ou une réponse cellulaire aux stress physiologiques ? Med Sci (Paris) 2005 ; 21 : 491–497. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]
  3. Olovnikov AM. A theory of marginotomy. The incomplete copying of template margin in enzymic synthesis of polynucleotides and biological significance of the phenomenon. J Theor Biol 1973 ; 41 : 181–190. [CrossRef] [PubMed] [Google Scholar]
  4. Stein GH, Dulic V. Origins of G1 arrest in senescent human fibroblasts. Bioessays 1995 ; 17 : 537–543. [CrossRef] [PubMed] [Google Scholar]
  5. D’Adda di Fagagna F, Reaper PM, Clay-Farrace L, et al. A DNA damage checkpoint response in telomere-initiated senescence. Nature 2003 ; 426 : 194–198. [CrossRef] [PubMed] [Google Scholar]
  6. Bischof O, Dejean A, Pineau P. Une revue de la sénescence cellulaire - Ami ou ennemi de la promotion tumorale ? Med Sci (Paris) 2009 ; 25 : 153–160. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]
  7. Shay JW, Pereira-Smith OM, Wright WE. A role for both RB and p53 in the regulation of human cellular senescence. Exp Cell Res 1991 ; 196 : 33–39. [CrossRef] [PubMed] [Google Scholar]
  8. Polager S, Ginsberg D. p53 and E2f: partners in life and death. Nat Rev Cancer 2009 ; 9 : 738–748. [CrossRef] [PubMed] [Google Scholar]
  9. Baus F, Gire V, Fisher D, et al. Permanent cell cycle exit in G2 phase after DNA damage in normal human fibroblasts. Embo J 2003 ; 22 : 3992–4002. [CrossRef] [PubMed] [Google Scholar]
  10. Chicas A, Wang X, Zhang C, et al. Dissecting the unique role of the retinoblastoma tumor suppressor during cellular senescence. Cancer Cell 2010 ; 17 : 376–387. [CrossRef] [PubMed] [Google Scholar]
  11. Vernier M, Bourdeau V, Gaumont-Leclerc MF, et al. Regulation of E2Fs and senescence by PML nuclear bodies. Genes Dev 2011 ; 25 : 41–50. [NASA ADS] [CrossRef] [EDP Sciences] [MathSciNet] [PubMed] [Google Scholar]
  12. Krishnamurthy J, Torrice C, Ramsey MR, et al. Ink4a/Arf expression is a biomarker of aging. J Clin Invest 2004 ; 114 : 1299–1307. [CrossRef] [PubMed] [Google Scholar]
  13. Baker DJ, Wijshake T, Tchkonia T, et al. Clearance of p16(Ink4a)-positive senescent cells delays ageing-associated disorders. Nature 2011 ; 479 : 232–236. [CrossRef] [PubMed] [Google Scholar]
  14. Gil J, Peters G. Regulation of the INK4b-ARF-INK4a tumour suppressor locus: all for one or one for all. Nat Rev Mol Cell Biol 2006 ; 7 : 667–677. [CrossRef] [PubMed] [Google Scholar]
  15. Herbig U, Jobling WA, Chen BP, et al. Telomere shortening triggers senescence of human cells through a pathway involving ATM, p53, and p21(CIP1), but not p16(INK4a). Mol Cell 2004 ; 14 : 501–513. [CrossRef] [PubMed] [Google Scholar]
  16. Kuilman T, Michaloglou C, Mooi WJ, Peeper DS. The essence of senescence. Genes Dev 2010 ; 24 : 2463–2479. [NASA ADS] [CrossRef] [EDP Sciences] [MathSciNet] [PubMed] [Google Scholar]
  17. Gorospe M, Abdelmohsen K. Microregulators come of age in senescence. Trends Genet 2011 ; 27 : 233–241. [CrossRef] [PubMed] [Google Scholar]
  18. Narita M, Nunez S, Heard E, et al. Rb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence. Cell 2003 ; 113 : 703–716. [CrossRef] [PubMed] [Google Scholar]
  19. Adams PD. Remodeling of chromatin structure in senescent cells and its potential impact on tumor suppression and aging. Gene 2007 ; 397 : 84–93. [CrossRef] [PubMed] [Google Scholar]
  20. Ferbeyre G, de Stanchina E, Querido E, et al. PML is induced by oncogenic ras and promotes premature senescence. Genes Dev 2000 ; 14 : 2015–2027. [NASA ADS] [CrossRef] [EDP Sciences] [MathSciNet] [PubMed] [Google Scholar]
  21. Kennedy AL, McBryan T, Enders GH, et al. Senescent mouse cells fail to overtly regulate the HIRA histone chaperone, do not form robust senescence associated heterochromatin foci. Cell Div 2010 ; 5 : 16. [CrossRef] [PubMed] [Google Scholar]
  22. Di Micco R, Sulli G, Dobreva M, et al. Interplay between oncogene-induced DNA damage response and heterochromatin in senescence and cancer. Nat Cell Biol 2011 ; 13 : 292–302. [CrossRef] [PubMed] [Google Scholar]
  23. Prieur A, Besnard E, Babled A, Lemaitre JM. p53, p16(INK4A) independent induction of senescence by chromatin-dependent alteration of S-phase progression. Nat Commun 2011 ; 2 : 473. [CrossRef] [PubMed] [Google Scholar]
  24. Rodier F, Campisi J. Four faces of cellular senescence. J Cell Biol 2011 ; 192 : 547–556. [CrossRef] [PubMed] [Google Scholar]
  25. Kuilman T, Michaloglou C, Vredeveld LC, et al. Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network. Cell 2008 ; 133 : 1019–1031. [CrossRef] [PubMed] [Google Scholar]
  26. Acosta JC, O’Loghlen A, Banito A, et al. Chemokine signaling via the CXCR2 receptor reinforces senescence. Cell 2008 ; 133 : 1006–1018. [CrossRef] [PubMed] [Google Scholar]
  27. Young AR, Narita M. Connecting autophagy to senescence in pathophysiology. Curr Opin Cell Biol 2010 ; 22 : 234–240. [CrossRef] [PubMed] [Google Scholar]
  28. Zoncu R, Efeyan A, Sabatini DM. mTOR: from growth signal integration to cancer, diabetes and ageing. Nat Rev Mol Cell Biol 2011 ; 12 : 21–35. [CrossRef] [PubMed] [Google Scholar]
  29. Demidenko ZN, Korotchkina LG, Gudkov AV, Blagosklonny MV. Paradoxical suppression of cellular senescence by p53. Proc Natl Acad Sci USA 2010 ; 107 : 9660–9664. [CrossRef] [Google Scholar]
  30. Pani G. From growing to secreting: New roles for mTOR in aging cells. Cell Cycle 2011 ; 10 : 2450–2453. [CrossRef] [PubMed] [Google Scholar]
  31. Narita M, Young AR, Arakawa S, et al. Spatial coupling of mTOR and autophagy augments secretory phenotypes. Science 2011 ; 332 : 966–970. [CrossRef] [PubMed] [Google Scholar]
  32. Collado M, Serrano M. Senescence in tumours: evidence from mice and humans. Nat Rev Cancer 2010 ; 10 : 51–57. [CrossRef] [PubMed] [Google Scholar]
  33. Michaloglou C, Vredeveld LC, Soengas MS, et al. BRAFE600-associated senescence-like cell cycle arrest of human naevi. Nature 2005 ; 436 : 720–724. [CrossRef] [PubMed] [Google Scholar]
  34. Bartkova J, Rezaei N, Liontos M, et al. Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints. Nature 2006 ; 444 : 633–637. [CrossRef] [PubMed] [Google Scholar]
  35. Krizhanovsky V, Yon M, Dickins RA, et al. Senescence of activated stellate cells limits liver fibrosis. Cell 2008 ; 134 : 657–667. [CrossRef] [PubMed] [Google Scholar]
  36. Nardella C, Clohessy JG, Alimonti A, Pandolfi PP. Pro-senescence therapy for cancer treatment. Nat Rev Cancer 2011 ; 11 : 503–511. [CrossRef] [PubMed] [Google Scholar]
  37. Coppe JP, Patil CK, Rodier F, et al. Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor. PLoS Biol 2008 ; 6 : 2853–2868. [PubMed] [Google Scholar]
  38. Adams PD. Healing and hurting: molecular mechanisms, functions, and pathologies of cellular senescence. Mol Cell 2009 ; 36 : 2–14. [CrossRef] [PubMed] [Google Scholar]
  39. Kang TW, Yevsa T, Woller N, et al. Senescence surveillance of pre-malignant hepatocytes limits liver cancer development. Nature 2011 ; 479 : 547–551. [CrossRef] [PubMed] [Google Scholar]
  40. Collado M, Blasco MA, Serrano M. Cellular senescence in cancer and aging. Cell 2007 ; 130 : 223–233. [CrossRef] [PubMed] [Google Scholar]
  41. Herbig U, Ferreira M, Condel L, et al. Cellular senescence in aging primates. Science 2006 ; 311 : 1257. [CrossRef] [PubMed] [Google Scholar]
  42. Rodier F, Coppe JP, Patil CK, et al. Persistent DNA damage signalling triggers senescence-associated inflammatory cytokine secretion. Nat Cell Biol 2009 ; 11 : 973–979. [CrossRef] [PubMed] [Google Scholar]
  43. Brondello JM, Philipot D, Djouad F, et al. Cellular senescence is a common characteristic shared by preneoplasic and osteo-arthritic tissue. Open Rheumatol J 2010 ; 4 : 10–14. [CrossRef] [PubMed] [Google Scholar]
  44. Serrano M, Blasco MA. Cancer and ageing: convergent and divergent mechanisms. Nat Rev Mol Cell Biol 2007 ; 8 : 715–722. [CrossRef] [PubMed] [Google Scholar]
  45. Lapasset L, Milhavet O, Prieur A, et al. Rejuvenating senescent and centenarian human cells by reprogramming through the pluripotent state. Genes Dev 2011 ; 25 : 2248–2253. [NASA ADS] [CrossRef] [EDP Sciences] [MathSciNet] [PubMed] [Google Scholar]
  46. Mudhasani R, Zhu Z, Hutvagner G, et al. Loss of miRNA biogenesis induces p19Arf-p53 signaling and senescence in primary cells. J Cell Biol 2008 ; 181 : 1055–1063. [CrossRef] [PubMed] [Google Scholar]
  47. Passos JF, Saretzki G, von Zglinicki T. DNA damage in telomeres and mitochondria during cellular senescence: is there a connection? Nucleic Acids Res 2007 ; 35 : 7505–7513. [CrossRef] [PubMed] [Google Scholar]
  48. Yoon YS, Yoon DS, Lim IK, et al. Formation of elongated giant mitochondria in DFO-induced cellular senescence: involvement of enhanced fusion process through modulation of Fis1. J Cell Physiol 2006 ; 209 : 468–480. [CrossRef] [PubMed] [Google Scholar]
  49. Lenaers G, Amati-Bonneau P, Delettre C, et al. De la levure aux maladies neurodégénératives - Dix ans d’exploration des pathologies de la dynamique mitochondriale. Med Sci (Paris) 2010 ; 26 : 836–841. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]
  50. Sahin E, Colla S, Liesa M, et al. Telomere dysfunction induces metabolic and mitochondrial compromise. Nature 2011 ; 470 : 359–365. [CrossRef] [PubMed] [Google Scholar]
  51. Lacroix M, Linares L, LeCam L. Le Yin et le Yang de la sénescence : est-il possible de vieillir sans développer de cancer ? Med Sci (Paris) 2012 ; 28 : 245–247. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]
  52. Rimmelé P, Zhang X, Ghaffari S. Rôle des facteurs de transcription FoxO dans la maintenance des cellules souches. Med Sci (Paris) 2012 ; 28 : 250–254. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]

Les statistiques affichées correspondent au cumul d'une part des vues des résumés de l'article et d'autre part des vues et téléchargements de l'article plein-texte (PDF, Full-HTML, ePub... selon les formats disponibles) sur la platefome Vision4Press.

Les statistiques sont disponibles avec un délai de 48 à 96 heures et sont mises à jour quotidiennement en semaine.

Le chargement des statistiques peut être long.